Saturday, December 29, 2007

WASHINGTON: Researchers, for the first time, have demonstrated in mice that a protein called brain-derived neurotrophic factor (BDNF) is critical in managing satiety, and is the main cause behind obesity and overeating.

The study, led by Maribel Rios, PhD, and assistant professor of neuroscience at the Sackler School of Graduate Biomedical Sciences at Tufts University School of Medicine in Boston and colleagues, revealed that it is the lack of BDNF that is responsible for triggering overeating and obesity.

Researchers showed that the mice in which the BDNF gene was deleted in two of the primary appetite-regulating regions of the brain ate more and became significantly heavier than their counterparts.

"Prior to this study, we knew that the global lack of BDNF and/or its receptor during development leads to overeating and obesity in young mice. However, it remained unclear and controversial whether BDNF mediated satiety in adult animals. Our recent findings demonstrate that BDNF synthesis in the ventromedial (VMH) and dorsomedial hypothalamus (DMH) is required for normal energy balance," said Rios.

"Additionally, because the mice examined in this study were genetically altered in adulthood, we were able to establish that BDNF acts as a satiety signal in the mature brain independently from its putative actions during development of the brain.

Boettiger recruited 24 subjects:19 provided fMRI data, 9 were recovering alcoholics in abstinence and 10 had no history of substance abuse. Another five were included in the genotyping analysis.

At the fMRI research facility at the University of California, Berkeley, financial decision tasks measured rational thinking and impulsivity. Sober alcoholics chose the "now" reward almost three times more often than the control group, reflecting more impulsive behavior.

While decisions were being made, the imaging detected activity in the posterior parietal cortex, the dorsal prefrontal cortex, the anterior temporal lobe and the orbital frontal cortex. People who sustain damage to the orbital frontal cortex generally suffer impaired judgment, manage money poorly and act impulsively, the scientists noted.

The study revealed reduced activity in the orbital frontal cortex in the brains of subjects who preferred "now" over "later," most of whom had a history of alcoholism.

The orbital frontal cortex activity may be a neural equivalent of long-term consequences, Fields said.

"Think of the orbital frontal cortex as the brakes," Boettiger explained. "With the brakes on, people choose for the future. Without the brakes they choose for the short-term gain."

The dorsal prefrontal cortex and the parietal cortex often form cooperative circuits, and this study found that high activity in both is associated with a bias toward choosing immediate rewards.

The frontal and parietal cortexes are also involved in working memory - being able to hold data in mind over a short delay. When asked to choose between $18 now or $20 in a month, the subjects had to calculate how much that $18 (or what it could buy now) would be worth in a month and then compare it to $20 and decide whether it would be worth the wait.

The parietal cortex and the dorsal prefrontal cortex were much more active in people unwilling to wait. This could mean, Boettiger said, that the area is working less efficiently in those people.

The researchers also focused on a variant of a gene called COMT. The mutation is associated with lower dopamine levels, and the study showed that people with two copies of this allele (resulting in the lowest dopamine levels) had significantly higher frontal and parietal activity and chose "now" over "later" significantly more often.

"We have a lot to learn," Boettiger said. "But the data takes a significant step toward being able to identify subtypes of alcoholics, which could help tailor treatments, and may provide earlier intervention for people who are at risk for developing addictions."

The bigger picture, she added, is that her study provides more evidence that addiction is a disease, something even some of her peers don't yet believe.

"It's not unlike chronic diseases, such as diabetes," she said. "There are underlying genetic and other biological factors, but the disease is triggered by the choices people make."

“Our data suggest there may be a cognitive difference in people with addictions. Their brains may not fully process the long-term consequences of their choices. They may compute information less efficiently,” said Boettiger, who led the study as a scientist at UCSF's Ernest Gallo Clinic and Research Center.

“What’s exciting about this study is that it suggests a new approach to therapy. We might prescribe medications, such as those used to treat Parkinson’s or early Alzheimer’s disease, or tailor cognitive therapy to improve executive function,” she added.

Dr. Howard Fields, the senior author of the study, said that the newly found link involving the gene, impulsive behaviour and brain activity suggests that raising dopamine levels may be an effective treatment for addiction.

“I am very excited about these results because of their clinical implications. The genetic findings raise the hopeful possibility that treatments aimed at raising dopamine levels could be effective treatments for some individuals with addictive disorders,” Fields said.

During the study, the subjects were asked either to choose less money then and there or to get more money later. Their brain activity was scanned using functional magnetic resonance imaging (fMRI), as the participants made their choices.

The researchers revealed that while decisions were being made, the imaging detected activity in the posterior parietal cortex, the dorsal prefrontal cortex, the anterior temporal lobe and the orbital frontal cortex.

They said that sober alcoholics tended to chose the “now” reward almost three times more often than the control group, reflecting more impulsive behaviour.

The authors noted that the imaging detected reduced activity in the orbital frontal cortex in the brains of subjects who preferred “now” over “later”, most of whom had a history of alcoholism.

“Think of the orbital frontal cortex as the brakes. With the brakes on, people choose for the future. Without the brakes they choose for the short-term gain,” Boettiger said.

The dorsal prefrontal cortex and the parietal cortex often form cooperative circuits, and the study found that high activity in both is associated with a bias toward choosing immediate rewards.

The study also showed that people with two copies of the mutation in a gene called COMT, which is associated with lower dopamine levels, had significantly higher frontal and parietal activity, and chose “now” over “later” significantly more often.

“We have a lot to learn. But the data takes a significant step toward being able to identify subtypes of alcoholics, which could help tailor treatments, and may provide earlier intervention for people who are at risk for developing addictions,” Boettiger said. (ANI)

LONDON: Is addiction a brain disease? Yes, if researchers are to be believed, because it changes the way the brain functions.

A team of international researchers has carried out a study and found that alcoholics and drug addicts are naturally more impulsive when compared to other normal people, The Daily Telegraph reported on Wednesday. According to lead researcher Charlotte Boettiger of the University of North Carolina, "Their (the addicts') brains may not fully process the long-term consequences of their choices."

The researchers came to the conclusion after carrying out brain scans on nine sober recovering alcoholics. The participants were given financial decision tasks that allowed them to choose “less money now” or “more money later”. The addicts chose the "now" reward almost three times as often.

In fact, the team found that they had less activity in the orbital frontal cortex - the part of the brain that helps people make wise long-term decisions - than volunteers with no history of addiction.

The researchers also found a genetic link with the brain chemical dopamine - they believe that raising dopamine levels may be a treatment for addiction. The results of their study have been published in the Journal of Neuroscience.

Lead researcher Charlotte Boettiger, assistant professor of psychology at the University of North Carolina at Chapel Hill, says that this mutation is already known to reduce brain levels of the neurotransmitter dopamine.

"Our data suggest there may be a cognitive difference in people with addictions. Their brains may not fully process the long-term consequences of their choices. They may compute information less efficiently," said Boettiger, who led the study as a scientist at UCSF's Ernest Gallo Clinic and Research Center.

"What's exciting about this study is that it suggests a new approach to therapy. We might prescribe medications, such as those used to treat Parkinson’s or early Alzheimer’s disease, or tailor cognitive therapy to improve executive function," she added.

Friday, December 28, 2007

New mechanism explains glucose effect on wakefulnessOne of the body's basic survival mechanisms is the neural machinery that triggers the hungry brain to the alertness needed for seeking food. That same machinery swings the other way after a hearty meal, as exemplified by the long and honored custom of the siesta. However, scientists have understood little about how the basic energy molecule, glucose, regulates such wakefulness and other energy-related behaviors.

Now, in an article in the June 1, 2006, Neuron, Denis Burdakov of the University of Manchester and his colleagues have pinpointed how glucose inhibits neurons that are key to regulating wakefulness. In the process, they have discovered a role for a class of potassium ion channels whose role has remained largely unknown. Such ion channels are porelike proteins in the cell membrane that affect cellular responses by controlling the flow of potassium into the cell.

The researchers set out to discover how glucose inhibits a particular class of glucose-sensing neurons that produce tiny proteins called orexins, which are central regulators of states of consciousness.

Burdakov and colleagues wrote, "These cells are critical for responding to the ever-changing body-energy state with finely orchestrated changes in arousal, food seeking, hormone release and metabolic rate to ensure that the brain always has adequate glucose."

Malfunction of orexin neurons can lead to narcolepsy and obesity, and researchers have also found evidence that orexin neurons play a role in learning, reward-seeking, and addiction, the researchers wrote.

"Considering these crucial roles of orexin neurons, their recently described inhibition by glucose is likely to have considerable implications for the regulation of states of consciousness and energy balance," wrote Burdakov and his colleagues. "However, as in other glucose-inhibited neurons, it is unknown how glucose suppresses the electrical activity of orexin cells." What's more, they wrote, "Because the sensitivity of orexin cell firing to the small changes in extracellular glucose that occur between normal meals has never been tested, the daily physiological relevance of their glucose sensing is also unknown."

ABSTRACTThe prevalence of obesity has increased dramatically in recent years in the United States, with similar patterns seen in several other countries. Although there are several potential explanations for this dramatic increase in obesity, dietary influences are a contributing factor. An inverse correlation between dietary sugar intake and body mass index has been reported, suggesting beneficial effects of carbohydrate intake on body mass index. In this review we discuss how sugars interact with regulatory neurochemicals in the brain to affect both energy intake and energy expenditure. These neurochemicals appear to be involved in dietary selection, and sugars and palatable substances affect neurochemical changes in the brain. For example, rats that drink sucrose solutions for 3 wk have major changes in neuronal activity in the limbic area of the brain, a region involved in pleasure and other emotions. We also investigate the relations between sucrose (and other sweet substances), drugs of abuse, and the mesolimbic dopaminergic system. The presence of sucrose in an animal’s cage can affect the animals desire to self-administer drugs of abuse. Also, an animal’s level of sucrose preference can predict its desire to self-administer cocaine. Such data suggest a relation between sweet taste and drug reward, although the relevance to humans is unclear. Finally, we address the influence of sugar on body weight control. For example, sucrose feeding for 2 wk decreases the efficiency of energy utilization and increases gene expression of uncoupling protein 3 in muscle, suggesting that sucrose may influence uncoupling protein 3 activity and contribute to changes in metabolic efficiency and thus regulation of body weight.

Sugars provide energy and a pleasant taste. It should not be surprising, therefore, that the intake of sugars is influenced by 2 types of brain systems: those associated with the regulation of feeding and energy homeostasis and those associated with reward. During the past 3 decades, it has become clear that a host of neuromodulators are involved in the regulation of both energy and reward pathways. Many of these substances increase feeding (orexigenic agents) or decrease feeding (anorexic agents), and some also affect energy expenditure. In this review we focus on how sugars interact with regulatory neurochemicals in the brain to affect both energy intake and energy expenditure. We also examine the relations between sucrose (and other sweet substances), drugs of abuse, and the mesolimbic dopaminergic system. Finally, we discuss the influence of sugar on body weight regulation.

[…]

NEUROCHEMICAL CHANGES INDUCED BY SUGARS

Several laboratories have published data suggesting that ingestion of sweet tastants results in neurochemical changes indicative of a change in opioid- or dopamine-mediated responses. Pomonis et al (36) gave rats access to a 10% sucrose solution or water for 3 wk and injected the rats with 10 mg naloxone or saline/kg. The rats’ brains were subsequently analyzed for c-Fos immunoreactivity in limbic and autonomic regions in the forebrain and hindbrain. c-Fos is an early gene transcription factor, and an increase in c-Fos concentrations is thought to reflect neural activation. Pomonis et al found that c-Fos concentrations in the central nucleus of the amygdala after naloxone injection were elevated more in the rats that drank 10% sucrose than in those that drank water. This suggests that this area is activated when sucrose is ingested. Thus, the central nucleus of the amygdala may participate in the integration of gustatory, hedonic, and autonomic signals as they relate to sucrose consumption.

Colantuoni et al (37) daily gave rats a 25% glucose solution with laboratory food pellets for 12 h, followed by 12 h of food deprivation. The rats doubled their glucose intake in 10 d and developed a pattern of excessive intake in the first hour of daily access. After 30 d, receptor binding in several brain areas of the glucose-exposed animals was compared with that in controls fed food pellets. Dopamine D-1 receptor binding increased significantly in the accumbens core and shell. In contrast, D-2 binding decreased in the dorsal striatum. Binding to dopamine transporter increased in the midbrain. Opioid mu-1 receptor binding increased significantly in the cingulate cortex, hippocampus, locus coeruleus, and accumbens shell. These data indicate neurochemical and region-specific responses to glucose intake and suggest a complex interplay between dopamine and opioids in the neural response to sugar. Colantuoni et al (38) also noted behavior changes associated with opiate withdrawal, such as teeth chattering in rats injected with naloxone after chronic glucose imbibition. Thus, chronic ingestion of sugars by laboratory animals may result in a state that resembles mild opioid dependence.

[…]

Sucrose and reward

Human studies on the predictive potential of sucrose intake or preference on subsequent drug intake are relatively scarce and obviously cannot be conducted in a manner that precisely parallels the design of animal studies. Because of the established genetic influence on alcoholism (eg, 49), several studies examined taste preferences in subjects at risk for the development of alcoholism. Kampov-Polevoy et al (45) reported that subjects with a paternal history of alcohol dependence had a greater preference for strong sucrose solutions than did subjects with no paternal history of alcohol dependence. On the other hand, Scinska et al (50) and Kranzler et al (51) found no difference in the liking of sweets between sons of male alcoholics and control subjects. Scinska et al (50) did, however, note some differences in sensitivity to or preferences for salty and sour tastes. Therefore, the status of sweet taste preference as a marker for alcoholism is unclear, and we are not aware of any human studies in which sucrose preferences have been studied as potential markers for any other type of substance abuse.

Concurrent access to sweetened solutions and drugs of abuseIn rats, the intake of alcohol solutions with a concentration {approx}6% is low (52), and sucrose is often added to alcohol solutions to facilitate intake (eg, 53). However, when sucrose is provided as an alternative to alcohol, alcohol intake is reduced (53, 54). This effect is not specific to sucrose, because reductions in alcohol intake have also been obtained by the provision of saccharin and fat (54, 55). Given the differences between fat, sucrose, and saccharin in terms of caloric value and postingestive consequences, one may speculate that palatability is the salient factor in causing a reduction in intake. The effect is also not limited to alcohol, because the availability of palatable substances has been shown to reduce the intakes of orally self-administered phencyclidine in monkeys (56) and amphetamine in rats (57). The intravenous self-administration of cocaine is reduced by the availability of a glucose or saccharin solution

[…]

EFFECTS OF SWEET SUBSTANCES ON THE MESOLIMBIC DOPAMINERGIC SYSTEM

The evidence reviewed above suggests a relation between sweet taste and drugs of abuse. Under certain laboratory conditions, a high preference for or intake of sweet-tasting substances can predict subsequent drug use, and the intake of these substances may modify the amount of drug self-administration. These relations may be consistent with the possibility that the rewarding effects of sweets and drugs of abuse are mediated by similar or overlapping mechanisms. The mesolimbic dopaminergic system is thought to play an important role in mediating the rewarding and incentive or motivational properties of drugs (68, 69). One effect common to many drugs of abuse is an increase in extracellular dopamine in the nucleus accumbens (69). The ingestion of food can also cause an increase in dopamine release in the nucleus accumbens, although, as pointed out by Wise (70), the effects are not as large as those produced by cocaine, heroin, or amphetamine.

Martel and Fantino (71) reported that the ingestion of a palatable food caused a greater increase in dopamine release than did the ingestion of standard laboratory food. However, a subsequent study indicated that this difference may have been due in part to differences in the amount consumed (72). When ingested in solution (73) or in granulated form (74), sucrose was also shown to increase dopamine release in the nucleus accumbens. Interestingly, increased dopamine release in response to granulated sugar was only observed in rats classified as high-sugar feeders; rats classified as low-sugar feeders did not have increased dopamine release (74). This difference, like that observed in the comparison between palatable food and usual laboratory food (71), may have been partially due to differences in intake during the microdialysis sessions. Similarly, the response to the ingestion of sucrose solution was compared with the response to water intake, and the different amounts of water and sucrose ingested may have been a factor (73). Nevertheless, these studies indicate some degree of activation by the ingestion of palatable food of the same system thought to be important in mediating drug reward. The observations that dopaminergic antagonists cause a reduction in the intake of sucrose solutions are also consistent with this view

Wow! What an interesting article. Carbs act in conjunction with brain chemicals to produce a kind of addiction, one that actually reshapes the brain and molds human behavior.

It sounds too good to be true, but many women with polycystic ovarian syndrome (PCOS) say that when they eat more vegetables and meats and less bread and fruit, they start ovulating and lose weight. As a result, a growing number of nutritionists and a few physicians are advocating so-called insulin-sensitizing diets, which are similar to the "protein power" regimes being promoted in many best-selling books.

When a healthy person eats a carbohydrate, insulin levels rise to break down the resulting sugar in the blood. But women with PCOS are insulin-resistant, meaning they have defective cells that hamper this metabolism and increase the risk of diabetes. In addition, to try to compensate for the defect, their bodies produce more and more insulin, which can damage the insulin-producing system.

To make matters worse, this excess of insulin can trigger bouts of hunger that lead to overeating and weight gains.

Proteins and fats, by contrast, do not spark the same insulin surge in women with PCOS. As a result, these nutrients are metabolized normally.

Most doctors treating PCOS do not advocate high-protein diets, and they warn their patients not to eliminate carbohydrates completely. Yet these same physicians acknowledge that many patients who change their eating habits do feel better – and some have even gotten pregnant without fertility treatments.I love this article! Well, these women used a low carb diet to cure an incurable disease, or at least ameliorate it enough to become pregnant, but skeptical doctors still not sure about a "high fat" diet! lol! If it works, it works! PCOS in associated with insulin insensitivity, facial hair and infertility in women, and ishelped by the same diet that helps people with metabolic syndrome, epilepsy, parkinson's, narcolepsy, cancer, obesity, etc. - the low carb, high fat diet.

It's also interesting to read about Cushings, this super complex adrenal problem in humans, cats and dogs. Only in domesticated animals and humans. Who eat a high carb diet of grains. Cured by either taking meds the rest of your life and having your adrenal gland removed, or just stop eating carbs. Docs still not sure on that one either, lol!

Monday, December 24, 2007

Have you been diagnosed with clinical depression? Heart disease? Type II, or adult, diabetes? Narcolepsy? Are you, or do you think you might be, an alcoholic? Do you gain weight around your middle in spite of faithfully dieting? Are you unable to lose weight? Does your child have ADHD? If you have any one of these symptoms, I wrote this article for you. Believe it or not, the same thing can cause all of the above symptoms.

I am not a medical professional. I am not a nutritionist. The conclusions I have drawn from my own experience and observations are not rocket science. A diagnosis of clinical depression is as ordinary as the common cold today. Prescriptions for Prozac, Zoloft, Wellbutrin, etc., are written every day. Genuine clinical depression is a very serious condition caused by serotonin levels in the brain. I am not certain, however, that every diagnosis of depression is the real thing. My guess is that about 10 percent of the people taking these drugs actually need them. I am not saying that the other 90 percent do not have real and very distressing symptoms! I am saying that I believe that 90 percent of the people diagnosed with clinical depression actually do have normal serotonin levels. They have a very real condition, all right, but it isn't depression.

The condition they have is called insulin resistance. Left untreated, it will cause weight gain (around the middle of the body) and depression-like symptoms. Over time, it will cause problems with concentration and alertness. In the worst cases, it will cause diabetes, heart disease, and eventually, death. The problem here is elementary physiology. The human body uses insulin to store glucose in cells (as fat). Most of us know that glucose is sugar, but very few of us know that the body cannot distinguish between starches and sugar. Your body cannot tell the difference between a piece of white bread and a handful of sugar. Whole wheat bread is better, but only because it is absorbed into the blood more slowly. All carbohydrates - including, but not limited to, rice, corn, potatoes, and even carrots - are converted into sugar in your body. In fact, there is a school of thought that says that a baked potato is actually worse for you than eating raw glucose. From my own experience, I think that school of thought is quite correct. In some people, particularly after years of abuse, the body stops utilizing insulin well. To compensate, the pancreas makes more insulin. The results include weight gain, an increase in triglycerides, lousy cholesterol ratios, climbing blood pressure. In extreme cases, the pancreas eventually becomes exhausted and insulin levels fall, creating Type II diabetes. In short, I am talking about a recipe for suicide.

Insulin resistance is deadly, but why does it also make you feel lousy? Blood sugar! First, you eat something that makes blood sugar rise - some sort of carbohydrate. Maybe it was a candy bar. Maybe it was a sandwich (two slices of bread!). Maybe it was a baked potato, or rice, or a serving of corn. Maybe it was a breakfast pastry or bowl of cereal. After you eat, blood sugar rises for about twenty minutes, which makes you feel quite good. Meanwhile, your body is busily trying to utilize this food. Wups! The insulin isn't working. Make more. And more. All of a sudden, you have too much insulin floating about and your blood sugar drops through the floor. You feel worse than sleepy. It's a groggy feeling, like you've taken a barbiturate - you can't keep your eyes open. If you can, you go to sleep. If you can't, you suffer. Either way, it's over eventually. Afterward, you actually have a slight hangover, like you've been poisoned. Well, your own body has poisoned you. Worse still, you are now ravenously hungry - so you do it again. If I have just described you, then you are insulin resistant and addicted to carbohydrates. It wasn't your fault. You did as you were told by the folks who should have known better. Don't beat yourself up about it. But it's going to kill you if you don't change it. The lousy feeling of low blood sugar mimics depression. That uncontrollable sleepiness mimics narcolepsy. But how does this explain alcoholism? As in the other two cases, it doesn't. Alcoholism, like clinical depression and narcolepsy, is a real and incurable disease. But carbohydrate addiction can certainly cause problem drinking! Nothing on this planet can be converted to pure sugar faster than alcohol, so nothing makes you feel better faster when your blood sugar is below the floor - very briefly. Then your blood sugar crashes, and you need another drink to feel better again. And another. And another. The next thing you know, you are looking at a DWI, which is totally bewildering because you did not set out to get drunk!

I would add that I think the mood problems stem not only from the quick spike in blood sugar, but over the longer term from the insulin resistance keeping sugar out of your muscles and brain and storing it all as fat instead. The worst of all possible worlds. There's also alot to be said for the many properties of cereal grains to affect our endocrine system in a negative way. Insulin resistance, specifically in the brain itself, is also a factor. I have many links on my blog to articles I've found tying many disorders to insulin resistance. Hope you stay and look around a bit!

Meanwhile, a new area of research shows that another brain chemical called orexin may play a key role in the drowsiness cycle, regardless of whether any turkey is on the plate.

Scientists have long known that when people are hungry, they are more alert. In prehistoric times, that was probably a signal for people to get off their duffs and start stalking the latest meal, as opposed to simply taking a short hike to the refrigerator.

Recent studies have shown that animals' brains secrete orexin when they are hungry and their baseline metabolism is low. Conversely, after a meal, when baseline metabolism rises and the animal gets sleepy, the output of orexin drops off.

Ever wonder why certain meals make you feel great, while others leave you feeling sluggish and ready to nap? The answer lies within the way that nutrients from these foods interact with brain chemicals to either enhance our levels of alertness and motivation or to make us sleepy.

Nutritionists have always known that meals comprised primarily of improper carbohydrates (such as fibre-void white bread) can cause us to feel less than energetic, while meals high in protein can help us feel alert. Research in the early ’80s performed at the Massachusetts Institute of Technology (MIT) showed that carbohydrates help elevate levels of a calming brain chemical called serotonin, the precursor to melatonin, also known as the hormone of sleep.

This research team also discovered that one of the main reasons we crave carbohydrates is to compensate for a reduction in serotonin levels. Carbohydrates elevate brain serotonin by stimulating insulin levels, which ultimately drive the amino acid tryptophan–the main building block of serotonin–into the brain. Since depression and stress can greatly deplete tryptophan levels, this is also believed to be one of the primary reasons we crave carbohydrates when we are feeling down or are experiencing excess stress.

It is also widely accepted that processed carbohydrates can cause wild blood sugar fluctuations, which may lead to hypoglycemic episodes (low blood sugar). Since your body operates in a very narrow blood sugar range, each time you consume high-glycemic carbs (carbs that release their sugars rapidly) you stimulate excess insulin production in order to balance the body. The problem is that insulin remains active even after blood sugar is lowered, causing your body to crave more sugar (carbs) in order to raise blood sugar levels once again–and so the vicious cycle repeats itself.

High-protein-containing meals tend to stimulate the brain rather than sedate it. Researchers have discovered a few main reasons for this. First, complete proteins (such as chicken, fish, and eggs) contain high levels of the amino acids phenylalanine and tyrosine, the building blocks of the brain-stimulating chemicals dopamine and norepinephrine. It is important to note that these proteins (along with three others) compete with tryptophan for entry into the brain, and more often than not win entry to help you feel more alert.

Another reason carbohydrates tend to decrease levels of alertness when compared to proteins is that their biological effects seem to block levels of a group of brain chemicals called orexins. Found within the hypothalamus portion of the brain, orexins work to enhance our levels of alertness. Researchers from the University of Manchester in England have discovered that even small increases in blood sugar levels can cause sleepiness by suppressing orexins.

The next time you grab a doughnut or croissant for breakfast, you will at least understand why you need that cup (or pot) of coffee just to get you through the morning. Instead, try mixing up a protein shake with fresh or frozen berries and some essential fats–your mind and body will thank you for it!

A large kindred affected by TS and identified two family members with TTD who are very likely obligate carriers of the TS gene. These tics are more noticeable during stressful, fatiguing or emotional times. Tics appear to get worse with emotional stress and do not occur during sleep. Tics increase in frequency and severity with stress, during relaxation after physical exercise, idleness, fatigue, exposure to heat, and use of dopaminergic drugs, such as steroids, caffeine, and CNS stimulants. Tics usually diminish with performance of engaging mental or physical activities or with consumption of marijuana, alcohol or nicotine. Some people can control the tic urges so that they only tic in the privacy of a safe place, such as their home. Tics are severe to cause problems in school or occupational functioning, then behavioral techniques are recommended. Tics may be precipitated in with ADHD when they are given methylphenidate (Ritalin).Causes of Transient Tic Disorder

For decades, doctors who have treated children with both attention deficit-hyperactivity disorder (ADHD) and tics have been warned not to prescribe methylphenidate (Ritalin), the most common drug for ADHD, because of a concern that it would make the tics worse. Now, the first randomized, placebo-controlled clinical trial of methylphenidate and another drug, clonidine (Catapres), has found that in fact these drugs do not adversely affect tics. The researchers also found that a combination of the drugs is more effective than either drug alone.

For decades, doctors who have treated children with both attention deficit-hyperactivity disorder (ADHD) and tics have been warned not to prescribe methylphenidate (Ritalin), the most common drug for ADHD, because of a concern that it would make the tics worse. Now, the first randomized, placebo-controlled clinical trial of methylphenidate and another drug, clonidine (Catapres), has found that in fact these drugs do not adversely affect tics. The researchers also found that a combination of the drugs is more effective than either drug alone.

The study showed that methylphenidate and clonidine are individually effective for treating ADHD in children with tics and that the two drugs help control different symptoms of ADHD, says Roger Kurlan, M.D., of the University of Rochester Medical Center in New York, who led the multicenter study. Methylphenidate primarily improved attentiveness and helped children stay "on task," while clonidine helped control hyperactivity and impulsivity. The study was supported in part by the National Institute of Neurological Disorders and Stroke (NINDS).

Most experts estimate that ADHD affects between 2 and 5 percent of children in kindergarten through grade 12, although some studies have suggested that those estimates are low. In Rochester, about a third of the children with ADHD also have tic disorders, although the tics in some children are very mild, Dr. Kurlan says. Studies have tied both ADHD and tics to problems in the brain's basal ganglia and in connections between the basal ganglia and the frontal lobes, which may explain why the two disorders often appear together, he adds.

Summary Anecdotal evidence links the initial phase of fasting or a low-carbohydrate diet with feelings of well-beingand mild euphoria. These feelings have often been attributed to ketosis, the production of ketone bodies which canreplace glucose as an energy source for the brain. One of these ketone bodies, b-hydroxybutyrate (BHB), is an isomer ofthe notorious drug of abuse, GHB (c-hydroxybutyrate). GHB is also of interest in relation to its potential as a treatmentfor alcohol and opiate dependence and narcolepsy-associated cataplexy. Here I hypothesize that, the mild euphoriaoften noted with fasting or low-carbohydrate diets may be due to shared actions of BHB and GHB on the brain.Specifically, I propose that BHB, like GHB, induces mild euphoria by being a weak partial agonist for GABABreceptors.I outline several approaches that would test the hypothesis, including receptor binding studies in cultured cells,perception studies in trained rodents, and psychometric testing and functional magnetic resonance imaging in humans.These and other studies investigating whether BHB and GHB share common effects on brain chemistry and mood aretimely and warranted, especially when considering their structural similarities and the popularity of ketogenic dietsand GHB as a drug of abuse.

Since recorded time, across many cultures, fastinghas been used in rituals aimed at attaining a higherstate of being. Fasting for religious and spiritualreasons has been mentioned in the Bible, bothOld and New Testaments, the Koran and the Mahabharata[1]. Anecdotal feelings of well-being andmild euphoria also litter the popular literature onlow-carbohydrate diets. For example, one diaristwrote after 2–3 days on the Atkin’s Diet: ‘‘It isnot an unpleasant feeling, a sort of mild, foggyeuphoria’’. [2]. From an evolutionary perspective,mild euphoria associated with short-term fastingmay ease anxiety and aid the search for food. Ketosisoccurs during the first few days of fasting or alow-carbohydrate diet, when breakdown of fat (boxidation)outstrips breakdown of carbohydrate(glycolysis). Three ketone bodies are produced bythe liver:

[..]

After 2–3 days of fasting BHB reachesmillimolar levels in the blood and brain [3], and togetherwith acetoacetate provides the brain withan alternative energy source to glucose. Severalbiochemical explanations have been proposed forthe feelings of euphoria often associated withshort-term total fasting or low-carbohydrate diets.Bloom [4] postulated that accumulation of acetoacetateproduces a mild intoxication similar to ethanol.Phillips [5] speculated from his studies indairy cows that the accumulation of isopropyl alcohol(a byproduct of acetone metabolism) in neuraltissue might be responsible for fasting-induced religious,mystical or hallucinatory experiences.HypothesisHere I propose that diet-induced euphoria may involveproduction of BHB, and may be at least partiallyexplained by the well-known psychologicaleffects of its isomer, c-hydroxybutyrate (GHB)(Fig. 1). Considering their structural similarities,it is perhaps surprising that no one has linked BHBand GHB before.

Unconventional wiring of the brain circuits that govern sleep and waking might explain the prevalence of insomnia and the condition's association with obesity, according to new work published in the April issue of Cell Metabolism. Characterized by a chronic inability to fall asleep or remain sleeping, insomnia is estimated to affect one in every eight Americans.

The researchers found that so-called hypocretin neurons--having important roles in both arousal and appetite--lack the ability of most neurons to filter "noise" from signal, reported Tamas Horvath and Xiao-Bing Gao of Yale University School of Medicine. The neurons also rapidly reorganize themselves, becoming even more excitable, in response to stresses such as food deprivation, they found.

"The cell bodies of most neurons act as a filter," sorting through a multitude of signals to eliminate noise and generate an appropriate response, Horvath said. "In contrast, it appears that the basic wiring of hypocretin neurons allows noise to become the major signal."

As obesity has reached epidemic proportions, the incidence of insomnia and sleep deprivation has also risen. Studies of this apparent insomnia-obesity association have suggested a causal link between the two, but the underlying mechanism has remained unclear. The new findings of hypocretin neurons offer some possible clues, Horvath said.

Neurotransmitter Orexin Associated With Pleasure And Reward Pathways In The Brain

ScienceDaily (Aug. 28, 2005) — Philadelphia, PA -- Researchers at the University of Pennsylvania School of Medicine have discovered that the recently identified neurotransmitter orexin (also known as hypocretin) influences reward processing by activating neurons in the lateral hypothalamus region of the brain. By identifying the relationship between orexin neurons and behaviors associated with reward seeking, drug relapse, and addiction, researchers hope to find new treatments for drug addiction.

[…]

Previous studies have linked orexin activity to sleep and arousal (wakefulness), as well as feeding and appetite. Anatomical studies have shown that orexin neurons extend into the brain regions associated with reward pathways, including the ventral tagmental area and nucleus accumbens. Communication between the lateral hypothalamus and these brain regions suggests that orexin neurons may have a role in motivation and reward-seeking behavior. In order to examine the relationship between orexin and reward seeking, Glenda Harris, PhD, working with Gary Aston-Jones, PhD, in the Department of Psychiatry at Penn, examined orexin function in rats using a behavioral test aimed at mimicking food- and drug-reward seeking and drug relapse. This research appeared online in Nature on August 14.

"The lateral hypothalamus has been tied to reward and pleasure for decades, but the specific circuits and chemicals involved have been elusive," says Aston-Jones. "This is the first indication that the neuropeptide orexin is a critical element in reward-seeking and drug addiction. These results provide a novel and specific target for developing new approaches to treat addiction, obesity, and other disorders associated with dysfunctional reward processing."

It's commonly known that a severe allergy to peanuts can cause death within minutes.What if there were an allergy that were delayed for hours and caused people to fall asleep instead? That is what I believe is happening in people with Narcolepsy.

Celiac disease is an allergy to gliadin, a specific gluten protein found in grains such as wheat, barley and rye. In celiac disease the IgA antigliadin antibody is produced after ingestion of gluten. It attacks the gluten, but also mistakenly binds to and creates an immune reaction in the cells of the small intestine causing severe damage. There is another form of gluten intolerance, Dermatitis Herpetiformis, in which the IgA antigliadin bind to proteins in the skin, causing blisters, itching and pain. This can occur without any signs of intestinal damage. Non-celiac gluten sensitivity is a similar autoimmune reaction to gliadin, however it usually involves the IgG form of the antibody and damage to the small intestine is not common. IgG antibodies are commonly associated with delayed food allergies.

It has recently been shown that certain IgG antigliadins bind to the protein Synapsin in the brain. I believe this starts a process which causes the cumulative loss of neurons producing the neurotransmitter orexin (also known as hypocretin) which causes narcolepsy.

This is some of the data which started my research:- Narcolepsy-like symptoms in mice have been induced by injecting them with antibodies from narcoleptic humans. No relationship between symptoms and anti-orexin antibodies has been found in narcoleptic patients however, which suggests the possibility that other antibodies are directed against the orexin cells.-Narcolepsy is strongly associated with an immune antigen gene DQB1*0602, appearing in 90% of patients.-HLA DQB1*06 alleles are also associated with Non-celiac gluten sensitivity. In fact DQB1*06 alleles seem to confer a higher risk to present neurological rather than intestinal symptoms.

This is the process I have proposed:1. Genetically susceptible people produce antigliadin antibodies capable of binding to brain proteins. These antibodies are ordinarily too large to pass through the blood-brain-barrier, and no damage occurs.2. The BBB is compromised somehow. Many narcolepsy patients contract mononucleosis sometime in their teens and this damages the barrier and then their symptoms start. Other infectious agents and chemicals such as anesthesia can also damage the membrane. There are also reports of sudden onset or rapid progression after head trauma.3. Antibodies infiltrate the brain, attach to the synapsin protein in the neurons, and obstruct neurotransmitter release. In narcolepsy the neurotransmitter is orexin, and it creates wakefulness and stimulates the dopamine cells elsewhere. Without orexin you fall asleep, and the lowered stimulation of the dopamine makes you depressed. This is why the attacks usually come in the afternoon. Gluten for breakfast starts the process, gluten for lunch clogs everything up, and a few hours later you can't stay awake. The problem is, the antibody lives for about 2 weeks. Every time you eat gluten you accumulate more of them in your brain.

4. This is not just a sleep disorder, it's progressive brain damage. The inability to release the neurotransmitter causes an excess of the protein alpha-synuclein in the cell. Alpha-synuclein is stiff and pointy and pokes holes in the cellular membranes like the nucleus, mitochondria and golgi complex, killing the cells. Autopsy examination of narcoleptics show they usually have NO orexin cells left.

Let me add two important points:

-The DBQ1*0602 allele is only the most commonly occurring gene in narcolepsy. It has been shown that other alleles also occur among narcoleptics, so do not assume because you have tested negative for this gene you are not gluten sensitive. There are many variants of antigliadin and no studies exist that determine which variants cause which symptoms. This mechanism also accounts for the less drastic symptoms of Idiopathic Hypersomnia.

[…]

The simple regimen of a gluten-free diet has been used effectively in the treatment of celiac disease. Strict adherence to a gluten-free diet arrests the progression of celiac disease, and long term compliance can result in healing of the small intestine and return to normal function. Early screening can prevent manifestation of the disease altogether. Similar results may be possible with the neurological effects of gluten sensitivity.

(In addition to myself, I do already have reports from 5 narcoleptics of positive tests, or rapid remission of their symptoms on a gluten-free diet.)

Personally I believe that anyone showing symptoms of narcolepsy, cataplexy, hypersomnia or major depression should be tested for gluten sensitivity. However, remember you can be gluten sensitive without having celiac disease. Celiac tests are specific for intestinal tissue antibodies and usually do NOT include an assay for IgG antigliadin. There are specific tests for gluten sensitivity which do include IgA and IgG antibodies. Your doctor may agree to order one for you, but as far as I can tell, most of them are only familiar with celiac disease and aren't aware of, or open to the possibility of neurological effects of gluten.

The above is from Heidi Lindborg's blog- the Kitchen Table. I've been thinking many of the same things based on learning about gluten, autoimmune diseases. I've been trying to connect the dots between obesity, ADD, diabetes, depression, circadian rhythyms, etc. and she's been doing the same thing. She has more links and articles, and lots of research on her blog, check it out!

Lahey & Carlson (1991) reviewed the research literature and concluded that was then called formerly called ADD was found in two independent dimensions:

1. one consisting of motor hyperactivity and impulsive behavior 2. the other consisting of inattention disorganization, and difficulty completing tasks

They concluded "it no longer seems doubtful that ADD/WO "exists," and that ADD without hyperactivity differs from ADD with hyperactivity in clinically important ways."

Brown & Gammon (1992, 1993) at Yale suggest that more is involved in ADHD without hyperactivity than just inattention. Such is not just a mild case of ADHD, but can be a debilitating disorder in which even bright and talented people are unable to activate themselves and sustain their efforts for productive work. What is called apathy or lack of motivation is a chronic problem with activation, which may be central to understanding this type of ADHD.

Many of those with non-hyperactive ADHD report chronic problems with "getting cranked up" to do tasks, even tasks they recognize as urgent and important for their own welfare. Often this activation problem in ADHD extends to sustaining energy for tasks. Many patients report great difficulty keeping up their energy to read or write or do a task. They speak of feeling drowsy even after a good night's sleep. Some almost meet the diagnostic category for narcolepsy, reporting problems with dozing at long stoplights and difficulty fighting off drowsiness while studying, listening to lectures, or attending meetings. There appears to be chronic difficulty not only in activating to work, but in sustaining energy for tasks.

Chronic problems in activating and sustaining arousal make life difficult for high-IQ people, who are seen by themselves, parents, teachers, and employers as extremely bright, with great promise for successful achievement. The symptoms of chronic inattention, lethargy, failure to follow through, brings oscillating achievement, poor grades and frequent reminders that "you could do much better if only you'd be more consistent." The wide gap between their potential and actual achievement can make these patients vulnerable to demoralization and resignation to failure.

The effects of a low-carbohydrate, ketogenic diet (LCKD) on sleepiness and other narcolepsy symptoms were studied. Nine patients with narcolepsy were asked to adhere to the Atkins’ diet plan, and their symptoms were assessed using the Narcolepsy Symptom Status Questionnaire (NSSQ). The NSSQ–Total score decreased by 18% from 161.9 to 133.5 (p = 0.0019) over 8 weeks. Patients with narcolepsy experienced modest improvements in daytime sleepiness on an LCKD.

Winfield, Ill., March 9, 2007—The impact of sleep deprivation in children and teenagers is an eye-opener, mimicking conditions ranging from attention-deficit disorder to adolescent depression to drunk driving.

Children who have trouble staying on task—distractible, fidgety, constantly moving—are often diagnosed with attention-deficit/hyperactivity disorder (ADHD), but may have actually have a sleep disorder, says Anna Ivanenko, MD, pediatric sleep medicine director at Central DuPage Hospital in Winfield.

“Studies have shown a clear link between sleep dysfunction, which causes excessive daytime sleepiness, and behavioral, mood and performance deficits,” says Dr. Ivanenko, who reported her findings recently at the second annual “Sleep and Learning” Seminar for DuPage County educators, sponsored by Central DuPage Hospital.

Children with sleep apnea, for instance, have a restless sleep, characterized by loud snoring, respiratory pauses and troubled breathing, sweating. Not surprisingly, they have trouble waking up in the morning, are sleepy during the day, and exhibit a wide range of behaviors usually associated with ADHD: hyperactivity, poor impulse control, aggressiveness, attention span problems, social withdrawal and learning problems, according to Dr. Ivanenko.

“Treating a child who has a sleep disorder and allowing him to get a good night’s sleep will frequently eliminate ADHD symptoms and the need for ADHD medication,” says Dr. Ivanenko.

· Adjusted to most schedules and lost its rhythm during sleep deprivation.

· When night sleep was reintroduced the noradrenaline rhythm reappeared while the existing adrenaline rhythm was accentuated.

(2) Exposure to a performance stressor at the trough raised adrenaline to daytime levels. An equally large response was seen at the peak.

(3) Interindividual [occurring between two and four individuals] day-to-day consistency of 3 and 24 hour levels was high for both catecholamines [neurotransmitters that activate--examples are dopamine, epinephrine and norepinephrine]. Intraindividual [being or occurring within the individual] consistency of the 24-hour pattern was high for adrenaline but low for noradrenaline. Cosine estimates of adrenaline phase showed a considerable intraindividual consistency while interindividual consistency was poor. Noradrenaline had poor cosine fit.

(4) Sleep deprivation did not change catecholamine excretion either during the vigil or during recovery sleep.

(5) It was concluded that adrenaline excretion, rated alertness, and body temperature exhibited self-sustained circadian rhythms which made adjustment to new sleep/wake patterns very difficult, and that the noradrenaline excretion rhythm depended on exogenous [outside the body] factors."

The human brain uses light not just to support vision but also to support alertness and cognitive tasks. Which colours of light are most effective and where in the brain these non-visual effects can be seen was previously not known. Now researchers at the Cyclotron Research Centre at the University of Liege and the Surrey Sleep Research Centre at the University of Surrey have ‘shed some novel light’ on these issues by using functional magnetic resonance (fMRI) brain imaging while the participant were engaged on a working memory task.

[…]

In a recent research paper it is reported that it is not just any light that is most effective but rather light of a particular short wavelength (480 nm, i.e. blue light rather than violet or green). This is in accordance with the hypothesis that such non-visual effects are mediated by a recently discovered ancient photoreceptor which is particularly sensitive to blue light.

More importantly maybe, by using very short exposures to light (< 1 minutes), in combination with brain imaging techniques, the researchers could identify the brain areas that are involved in the initial responses to this light. The brain areas that responded to blue light exposures included areas in the brain stem and the thalamus. These areas are involved in the regulation of very basic aspects of brain function, such as the regulation of alertness and sleepiness.

Other areas that responded to light included the hippocampus and amygdala. These areas are well known to be involved in the regulation of higher functions such as memory and emotion. In summary, these data establish a brain basis for the wide ranging effects of light on how we perform and feel. The data have implications for the development of better artificial light environments and a better understanding of the effects of light on the human brain in general.

Dr Gilles Vandewalle, lead author, comments that ‘ it was impressive to see how only a minor difference in wavelength could have such a dramatically different effect on our fMRI results’. Dr Pierre Maquet co-senior author, comments that ’ as a neurologist I am impressed by the wide ranging effects of light on brain function and the range of brain areas that are affected.

This is an area that certainly warrants further investigation.’ Dr Derk-Jan Dijk, co-senior author remarks, ‘ Humans are day-active animals, and maybe it is after all not so surprising to a biologist that blue light has these profound effects on our brain. After all, natural daylight contains quite a bit of blue light. We had simply forgotten about it because we are so preoccupied by the ‘visual’ effects of light, which are not particularly dependent on blue light. We now know that other aspects of brain function are.

Researchers from Brigham and Women's Hospital (BWH) in Boston and Jefferson Medical College have found that the body's natural biological clock is more sensitive to shorter wavelength blue light than it is to the longer wavelength green light, which is needed to see.

[…]

The discovery proves what scientists have suspected over the last decade: a second, non-visual photoreceptor system drives the body's internal clock, which sets sleep patterns and other physiological and behavioral functions.

"This discovery will have an immediate impact on the therapeutic use of light for treating winter depression and circadian disorders," says George Brainard, Ph.D., professor of neurology at Jefferson Medical College of Thomas Jefferson University in Philadelphia. "Some makers of light therapy equipment are developing prototypes with enhanced blue light stimuli."

"In the long range, we think this will shape all artificial lighting, whether it's used for therapeutic purposes, or for normal illumination of workplaces, hospitals or homes – this is where the impact will be," he says. "Broad changes in general architectural lighting may take years, but the groundwork has been laid."

In theory, he says, "If a clinician wants to use light therapeutically, the blue wavelengths may be more effective. If you wanted built-in illumination that would enhance circadian regulation, you might want this wavelength region emphasized. It is interesting that natural daylight – the blue sky – is rich in this part of the spectrum."

Scientists at John Carroll University, working in its Lighting Innovations Institute, have developed an affordable accessory that appears to reduce the symptoms of ADHD. Their discovery also has also been shown to improve sleep patterns among people who have difficulty falling asleep. The John Carroll researchers have created glasses designed to block blue light, therefore altering a person's circadian rhythm, which leads to improvement in ADHD symptoms and sleep disorders.

[…]

How the Glasses Work

The individual puts on the glasses a couple of hours ahead of bedtime, advancing the circadian rhythm. The special glasses block the blue rays that cause a delay in the start of the flow of melatonin, the sleep hormone. Normally, melatonin flow doesn't begin until after the individual goes into darkness.

Studies indicate that promoting the earlier release of melatonin results in a marked decline of ADHD symptoms.

A possible link between lack of sleep (insomnia) and obesity has been traced to hypocretin/orexin cells in the hypothalamus region of the brain that are easily excited and sensitive to stress, Yale School of Medicine researchers report in the April issue of Cell Metabolism.

"If these neurons are over-activated by environmental or mental stress in daily situations, they may support sustained arousal, triggering sleeplessness, leading to overeating," said lead author Tamas Horvath, associate professor in the Departments of Obstetrics, Gynecology & Reproductive Sciences (Ob/Gyn) and Neurobiology at Yale School of Medicine. "The more stress you have, the lower the threshold becomes for exciting these hypocretin neurons."

[…]

They found a unique, previously un-described organization of inputs on hypocretin neurons in which excitatory nerve junctions outnumber inhibitory contacts by almost 10 fold. Stressors such as fasting further excite these neurons.

"This unique wiring and acute stress-induced plasticity of the hypocretin neurons correlates well with its involvement in the control of arousal and alertness, which are vital to survival," said Horvath. "But it may also be an underlying cause of insomnia and associated metabolic disturbances, including obesity.

[…]

Previous studies demonstrated the association between lack of sleep and obesity and suggested a good night's sleep to help obesity. Horvath found that the neurological basis of the link between obesity and insomnia make them both independent and related products of the overactivated hypocretin system. Therefore, he said, "people with weight and sleep problems could benefit from cutting back on stressful aspects of their lives, rather than trying to specifically medicate either insomnia or obesity."

This article talks about overarousal, excitability and insomnia. What about underarousal? As in narcolepsy- which is seen as a problem with low orexin. Also- the "stress" from fasting- perhaps it is the opposite- the foods we eat (high carb) interfere with orexin. No food causes reversal. When I fast I have more energy. There's a lot to digest here.

Sunday, December 23, 2007

The rise of armed Sunni groups — who now battle al-Qaida in Iraq instead of fighting U.S. troops — is widely seen as a major reason for a drop in violence across the country.

But bringing these fighters into the fold of Iraq's security forces — and sparking a political reconciliation that will allow more Sunnis to participate in the governing process — is something the Shiite-dominated government is not adequately addressing, analysts say.

Iraqi officials report the number of fighters in the so-called "awakening" councils as about 70,000 and rapidly growing. They expect the number of Sunni fighters in Baghdad alone to grow to 45,000 next year — a fourfold increase from present figures.

By comparison, the Shiite dominated army and police make up the majority of the 440,000 Iraqi security forces.

Shiite government officials have in recent weeks cautiously praised the fighters for helping reduce violence. But laced into the comments were warnings that represent Shiites' biggest fear: that these groups will become an uncontrollable force and eventually use their guns to escalate a sectarian war that has largely divided Iraq into blocs along religious lines.

"The awakening movement was a response to al-Qaida in Iraq trying to prevent Sunnis from entering the political process," Defense Minister Abdul-Qader al-Obeidi, himself a Sunni Arab, said at a news conference on Saturday.

"The Sunnis' response was an uprising, represented by the awakening groups. Now that al-Qaida has largely been marginalized in certain areas, Sunnis are entering the political arena," al-Obeidi said. "We will see a definite change soon because there is nobody now standing between them and the rest of the Iraqi people."

Friday, December 21, 2007

Alan D. Lieberson, a medical doctor, lawyer, and the author of Treatment of Pain and Suffering in the Terminally Ill and Advance Medical Directives, explains.

The duration of survival without food is greatly influenced by factors such as body weight, genetic variation, other health considerations and, most importantly, the presence or absence of dehydration.

For total starvation in healthy individuals receiving adequate hydration, reliable data on survival are hard to obtain. At the age of 74 and already slight of build, Mahatma Gandhi, the famous nonviolent campaigner for India's independence, survived 21 days of total starvation while only allowing himself sips of water. In a 1997 article in the British Medical Journal, Michael Peel, senior medical examiner at the Medical Foundation for the Care of Victims of Torture, cites well-documented studies reporting survivals of other hunger strikers for 28, 36, 38 and 40 days. Most other reports of long-term survival of total starvation, however, have been poorly substantiated. [Editor's Note: Reports of the 1981 hunger strike by political prisoners against the British presence in Northeast Ireland indicate that 10 individuals died after periods of between 46 and 73 days without food.]

Unlike total starvation, near-total starvation with continued hydration has occurred frequently, both in history and in patients under medical supervision. Survival for many months to years is common in concentration camps and during famines, but the unknown caloric intake during these times makes it impossible to predict survival. What is evident is that the body can moderate metabolism to conserve energy and that individual survival varies markedly. The body's ability to alter its metabolism is poorly understood, but it occurs at least in part through changes in thyroid function. This may help explain the evolutionary persistence of genes causing diabetes, which in the past could have allowed individuals to survive periods of starvation by enabling more economical use of energy.

A gene variant involved in dopamine transmission may be linked to a binge-eating syndrome in seasonal affective disorder. The finding may point toward detection and prevention strategies.

Although only a small percentage of North Americans experience full-blown seasonal affective disorder—about 1 percent of Americans and 2 percent of Canadians—a much larger percentage—between 10 percent and 15 percent—report depression accompanied by increased eating and weight gain during the fall and winter. Moreover, of this larger percentage, a substantial number also engage in binge eating.

Now a gene variant linked to seasonal affective disorder binge eating appears to have been identified. It is a variant of the dopamine-4 receptor gene called the seven-repeat allele.

The study was headed by Robert Levitan, M.D., an associate professor of psychiatry at the University of Toronto. Results appeared in the November 2004 Biological Psychiatry. "Pending replication in other samples," the scientists wrote, "these results point to a genetic vulnerability factor that could help in the early identification and treatment of women at higher risk for seasonal weight gain associated with binge-eating behavior."

The dopamine-4 receptors appear to be active in limbic areas of the brain involved in cognition and emotion. There are seven known variants of the gene that codes for these receptors; the seven-repeat allele is one. Between 25 percent and 35 percent of Caucasians and up to 65 percent of some American-Indian populations possess at least one copy of this version.

Levitan and his colleagues previously found a link between the seven-repeat allele and obesity in women with seasonal affective disorder, implying that the allele might bring about weight gain via binge eating. They then undertook another study to investigate this hypothesis.

Characteristic symptoms of SAD are those of depression, which include dysphoria, feeling low, decreased in energy and activity, increased irritability, concentration difficulties, anxiety, decreased libido and social withdrawal. Unlike classically depressed patients, most SAD patients develop ‘atypical’ symptoms of increased fatigue, increased sleep duration and increased appetite and weight. Not only do SAD patients crave carbohydrates, but also they actually report eating more carbohydrate-rich foods in the winter1.

A study point out that patients are more disturbed by the lethargy and fatigue than by the mood changes themselves, especially in the early phases of their winter depression, therefore often seeking the help of a physician rather than a psychiatrist6. Untreated, SAD episodes generally resolve by springtime, although some do not fully recover before the early summer. Many patients reported that travel to latitudes nearer the equator resulted in remission or diminishing of their symptoms3.

Winter SAD is also seen in children, who present with fatigue, irritability, difficulty getting out of bed in the morning and school problems7. The seasonal pattern of summer is opposite to that of winter SAD with reversal of their winter symptoms in summer.

Wednesday, December 19, 2007

The last decade has seen medical care for ADHD grow into a huge industry. But it doesn't pretend to cure the problem, merely the symptoms.

Yet the most common finding in children with ADHD is hypoglycaemia (low blood sugar), and that is caused by a high-carb diet. When individuals have a low blood sugar response, the body releases adrenaline to raise blood sugar levels. In children, this may cause them to act aggressively.

Food helps some people with ADHD to feel calm. But the foods most eaten are those rich in sugar and other carbohydrates such as sweets, cakes, pasta and fruit.

Dr. Benjamin Feingold, a California paediatrician, noticed that many hyperactive children became excited after eating foods containing high concentrations of salicylates. These occur naturally in many fruits and vegetables and are especially concentrated in grapes, raisins, nuts, apples, and oranges. A study performed at the Hospital for Sick Children in London, published in the British journal, Lancet, demonstrated that most children with severe ADHD are salicylate sensitive, but that 90% of these children have additional food allergies.[x] These included: cow's milk products, corn (an additive in many prepared foods), eggs, wheat, and soya.

Other lines of research point to high levels of seed-sourced omega-6 fatty acids such as are found in margarines and cooking oils, which unbalance omega-6 to omega-3 ratios;[xi] and a number of chemical food additives.

Considering the whole weight of evidence, cutting out processed 'convenience' foods will avoid almost all the probable causes of ADHD. This is a much healthier way to treat ADHD than with drugs. ADHD could really be 'A Demand for a Healthy Diet'.

The Scrooges of this world now have an excuse for holding on to their money.

Generosity is determined by our genes, according to scientists.

Research suggests that those with a variant of a certain gene are significantly more likely to give their money away.

To study the phenomenon, a game was created called The Dictator in which more than 200 online participants were each given £6.

The players could either keep it or give it to other players who remained anonymous.

They were not told to what use the money would be put in case it influenced their decisions.

After taking samples of the players' DNA code, it was found that those with a certain variation of a gene called AVPR1a were 50 per cent more likely to give the money away.

Dr Ariel Knafo, who led the research at the Hebrew University in Jerusalem said: "This is the first evidence, to my knowledge, for a relationship between DNA and altruism or generosity.

"This is a really exciting discovery. You often hear it said that people are generous by nature.

"Well, we now know that's because it is encoded into their genes. We don't know yet why some people have this gene variation or how many people have it."

AVPR1a affects generosity by allowing a hormone called arginine vasopressin to affect brain cells. More generous people have a longer section of the gene, called its promoter, which makes it more active.

In addition, those found to have the longer version of the gene were found to score higher in a psychological test of generosity and were more likely to believe in values such as world peace, social justice and protecting the environment.

The study is published in the journal Genes, Brain and Behaviour. A lecturer in psychology at Buckinghamshire University, Dr George Fieldman, said there was good evidence that generosity could be inherited.

As altruism and good deeds promote social bonding, they lead to greater social success as others were more likely to reciprocate them.

He said: "People who have this generosity gene will tend to be good team players at work. They are generous with their time and the help they give to colleagues.

"As a result, they will be more successful in society. And for humans, social success is essential.

"It goes back to when man was a hunter-gatherer. Early men discovered that by working together they could hunt and kill more animals, and so the gene has evolved.

"If you work well as part of a team, there is a good chance you are also a generous person."

Sunday, December 16, 2007

Scientists at the University of Cambridge have discovered why some individuals may be predisposed to drug addiction and believe it may lead to better treatments for this brain disorder.

The new findings, published in today's edition of Science, may lead to more targeted treatments for addiction and other compulsive behaviour disorders with fewer side effects than current alternatives.

Certain changes in brain chemistry have been linked with drug addiction in humans. However, previous studies were unable to conclude whether individuals were predisposed to drug addiction because of these chemical changes or if chronic drug use itself caused the chemical changes in the brain.

Dr Jeff Dalley and colleagues, at the Behavioural and Clinical Neuroscience Institute, may have resolved this debate by demonstrating that changes in a neurotransmitter receptor in a particular part of the brain actually pre-dates drug use. Using positron emission tomography (a PET scan), they discovered that rats that were behaviourally impulsive, but which had not been exposed to drugs, had significantly less brain dopamine receptors than their more restrained counterparts. Additionally, these same impulsive rats were found to be considerably more likely to self-administer cocaine intravenously, thus linking impulsive behaviour with drug addiction vulnerability.

Dr Dalley's research, funded by the Medical Research Council and the Wellcome Trust, demonstrates that the changes in dopamine receptors and impulsivity pre-date drug use and do not emerge as a result of prolonged addiction. His findings may have important ramifications for a range of addictive substances, including nicotine and opiates, where high consumption rates have also been linked to a similar reduction in this particular brain receptor.

Dr Dalley said, "The next step is identifying the gene or genes that cause this diminished supply of brain receptors. This may provide important new leads in the search for improved therapies for attention deficit/hyperactivity disorder (ADHD) and compulsive brain disorders such as drug addiction and pathological gambling."

This article cites new proof low dopamine is involved in addiction. I have another article right before this one where brain scan evidence brings new proof low dopamine is involved in ADD/ADHD. ADD'ers have problems with addictions as well.

Legend has it, famed Russian and psychologist and researcher, Bluma Zeigarnik, was sitting at a café in Vienna when she noticed that her waiter could remember the details of a large order perfectly until that customer was served. Once served, the order literally vanished from the waiter’s memory.

Through further research, Zeigarnik discovered that people, in general, will remember the details of most any task until it is completed and then, remarkably, forget much of what unfolded. Moreover, once begun, there is an underlying psychological drive to complete the task.

So, between the process of remembering what needs to be done and enduring the constant tug to bring a task to completion, every unfinished task stakes a claim to a small piece of our memory and short-term cognitive abilities.

It stands to reason, then, that the more we begin and the less we finish, the more chronically occupied our minds become. Beyond feeling stressed, frazzled and overwhelmed, this can also lead to impaired thinking, problem-solving and creativity. Not the most pleasant state in the world.

[…] from another article by the same blogger......[…]

In my recent article on non-finishing, I talked about something called the Zeigarnick Effect, a phenomenon where you remember the details of a task until it is completed and then promptly forget it all. It’s like completing the task wipes your mental slate clean. Similarly, when you write down the unfinished tasks that are swirling around your mind and detail not only their current status, but critical task need for completion, you create a significant amount of mental “space.” This space go a long way toward returning you to a calmer place.

Meditation is being recommended by more and more physicians as a way to prevent, slow or at least control the pain of chronic diseases like heart conditions, AIDS, cancer and infertility. It is also being used to restore balance in the face of such psychiatric disturbances as depression, hyperactivity and attention-deficit disorder (ADD). In a confluence of Eastern mysticism and Western science, doctors are embracing meditation not because they think it's hip or cool but because scientific studies are beginning to show that it works, particularly for stress-related conditions. "For 30 years meditation research has told us that it works beautifully as an antidote to stress," says Daniel Goleman, author of Destructive Emotions, a conversation among the Dalai Lama and a group of neuroscientists. "But what's exciting about the new research is how meditation can train the mind and reshape the brain." Tests using the most sophisticated imaging techniques suggest that it can actually reset the brain, changing the point at which a traffic jam, for instance, sets the blood boiling. Plus, compared with surgery, sitting on a cushion is really cheap.

As meditation is demystified and mainstreamed, the methods have become more streamlined. There's less incense burning today, but there remains a nugget of Buddhist philosophy: the belief that by sitting in silence for 10 minutes to 40 minutes a day and actively concentrating on a breath or a word or an image, you can train yourself to focus on the present over the past and the future, transcending reality by fully accepting it. In its most modern, Americanized forms, it has dropped the creepy mantra bit that has you memorize a secret phrase or syllable; instead you focus on a sound or on your breathing. It's a practice of repetition found somewhere in the history of most religions. There are dozens of flavors, from the Relaxation Response to gtum-mo, a technique practiced by Tibetan monks in eight-hour sessions that allows them to drive their core body temperature high enough to overcome earthly defilements or—even cooler—to dry wet sheets on their backs in the freezing temperatures of the Himalayas.

The brain, like the body, also undergoes subtle changes during deep meditation. The first scientific studies, in the '60s and '70s, basically proved that meditators are really, really focused. In India a researcher named B.K. Anand found that yogis could meditate themselves into trances so deep that they didn't react when hot test tubes were pressed against their arms. In Japan a scientist named T. Hirai showed that Zen meditators were so focused on the moment that they never habituated themselves to the sound of a ticking clock (most people eventually block out the noise, but the meditators kept hearing it for hours). Another study showed that master meditators, unlike marksmen, don't flinch at the sound of a gunshot. None of this, oddly, has been duplicated for a Vegas show.

In 1967 Dr. Herbert Benson, a professor of medicine at Harvard Medical School, afraid of looking too flaky, waited until late at night to sneak 36 transcendental meditators into his lab to measure their heart rate, blood pressure, skin temperature and rectal temperature. He found that when they meditated, they used 17% less oxygen, lowered their heart rates by three beats a minute and increased their theta brain waves—the ones that appear right before sleep—without slipping into the brain-wave pattern of actual sleep. In his 1970s best seller, The Relaxation Response, Benson, who founded the Mind/Body Medical Institute, argued that meditators counteracted the stress-induced fight-or-flight response and achieved a calmer, happier state. "All I've done," says Benson, "is put a biological explanation on techniques that people have been utilizing for thousands of years."

While genetic background and diet interact to potentiate the insulin resistance syndrome, it is the neuroendocrine axis that regulates gene expression and the impact of diet to control overall metabolism. Research indicates important roles for temporal shifts in circadian rhythms of hypothalamic neurochemistry in the development of the insulin resistance syndrome.

Marked annual cycles between the obese, insulin resistant and lean, insulin sensitive states are well preserved across evolutionary time among vertebrate species in the wild and these seasonal shifts occur without any change in genome and cannot be explained fully by changes in caloric intake. A key element in this endogenous metabolic shift control-system is hypothalamic circadian dopamine neurophysiology. Endogenous increases in hypothalamic dopamine activity at particular times of day function to initiate a hypothalamic neurophysiology operative in the reversal of the insulin resistance syndrome.

By mimicking the neuroendocrine dopaminergic activation driving the seasonal shift to the lean, insulin sensitive state it is possible to produce such shifts in metabolism among a wide variety of genetic and dietary induced animal models of insulin resistance as well.

Such findings have spawned clinical investigations of bromocriptine, a dopamine D2 receptor agonist, for the treatment of metabolicdisease, particularly cardiometabolic risk.

This symposium will review published data on a) preclinical studies of hypothalamic dopaminergic activities operative in the reversal of the insulin resistance syndrome and related metabolic disease and b) clinical studies demonstratingthe potential utility of hypothalamic dopamine neuromodulation in the treatment or prevention of insulin resistance syndrome, cardiovascular disease and type 2 diabetes.Veroscience is apparently connecting the dots between circadian rhythm, dopamine, and insulin resistance. See the book "sleep sugar and survival" by ts wiley for details.

Insulin, long known as an important regulator of blood glucose levels, now has a newly appreciated role in the brain.

Vanderbilt University Medical Center researchers, working with colleagues in Texas, have found that insulin levels affect the brain's dopamine systems, which are involved in drug addiction and many neuropsychiatric conditions.

In addition to suggesting potential new targets for treating drug abuse, the findings raise questions as to whether improper control of insulin levels - as in diabetes - may impact risk for attention deficit hyperactivity disorder (ADHD) or influence the effectiveness of current ADHD medications.

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Working with Galli and Avison, Jason Williams, Ph.D., used fMRI to demonstrate that in normal, healthy rats with plenty of insulin, amphetamine increased neural activity in the striatum. But in diabetic animals, activity in the striatum was suppressed.

"This finding is in vivo evidence that, in the intact diabetic rat, loss of insulin has compromised DAT trafficking to the plasma membrane," Avison said. "These experiments show that there is likely a strong interplay between these important dopamine neurotransmitter systems and insulin signaling mechanisms, which we know are altered in diabetes"

The results are some of the first to link insulin status and dopaminergic brain function and hold several implications for human health and disease.

"This is really the first mechanistic connection in vivo between diabetes and amphetamine action," Galli said. "This offers a completely new perspective on the influence of this disease (diabetes) on brain function, as well as diseases with altered dopamine signaling, such as schizophrenia and ADHD."

Learning from mistakes may be, in part, a matter of genetics.New research shows that a certain gene glitch may make it harder to learn from negative feedback.That gene glitch affects the number of receptors for the brain chemical dopamine.Dopamine parks at dopamine receptors to do its job. Having fewer dopamine receptors is like having fewer parking spots at work -- you can't do your job if you're circling, looking for a parking spot.

[...]

Men with fewer dopamine receptors were less responsive than the other men to negative feedback. But all of the men were good at learning from positive feedback.The findings may shed new light on the link between fewer dopamine receptors and risky habits such as addiction and compulsive gambling, write the researchers.

ScienceDaily (Dec. 10, 2007) — Bipolar disorder, commonly known as manic-depressive disorder, is highly influenced by the circadian system -- the body's internal clock -- and a specific kind of psychotherapy may help decrease irregularities in the circadian system that can trigger key symptoms of bipolar disorder, according to a study presented today at the American College of Neuropsychopharmacology (ACNP) annual meeting. The results are important because they show for the first time that psychotherapy which focuses on practical lifestyle changes can ease the symptoms of bipolar disorder. Every year nearly six million American adults suffer from bipolar disorder, a brain disorder which causes severe shifts in mood, energy, and ability to function, according to the National Institute of Mental Health.

Maintaining a consistent sleep schedule and wake time can help balance the circadian system, which in turn can help people avoid nighttime sleeplessness or daytime exhaustion, which can increase the risk of new episodes of mania or depression. "Having already found that disruption in daily routines can make individuals with bipolar disorder vulnerable to new episodes of illness, we have now learned that working with patients to achieve and maintain regular social rhythms -- including regular sleep patterns and adequate physical activity -- will help to protect them against episodes of mania or depression," says Ellen Frank, Ph.D., clinical psychologist and professor of psychiatry and psychology at the University of Pittsburgh School of Medicine.

People with bipolar disorder tend to have extremely sensitive circadian systems, which makes it much more difficult for them to recover from disruptions in sleep and routine. In contrast, people without bipolar disorder generally recover fairly quickly if their systems are thrown off by a change in routine or loss of sleep and might even be temporarily energized by these alterations.

[...]

In a related study presented at the meeting, researchers studying circadian rhythms in mice found that the genes that regulate these rhythms also control the activity of neurons in the brain that utilize dopamine, a neurotransmitter implicated in motivation and emotion. Mice that are lacking some of the key circadian genes closely resemble bipolar patients in the manic state.

WASHINGTON (Reuters) - Human evolution has been moving at breakneck speed in the past several thousand years, far from plodding along as some scientists had thought, researchers said on Monday.

In fact, people today are genetically more different from people living 5,000 years ago than those humans were different from the Neanderthals who vanished 30,000 years ago, according to anthropologist John Hawks of the University of Wisconsin.

The genetic changes have related to numerous different human characteristics, the researchers said.

Many of the recent genetic changes reflect differences in the human diet brought on by agriculture, as well as resistance to epidemic diseases that became mass killers following the growth of human civilizations, the researchers said.

For example, Africans have new genes providing resistance to malaria. In Europeans, there is a gene that makes them better able to digest milk as adults. In Asians, there is a gene that makes ear wax more dry.

The changes have been driven by the colossal growth in the human population -- from a few million to 6.5 billion in the past 10,000 years -- with people moving into new environments to which they needed to adapt, added Henry Harpending, a University of Utah anthropologist.

"The central finding is that human evolution is happening very fast -- faster than any of us thought," Harpending said in a telephone interview.

"Most of the acceleration is in the last 10,000 years, basically corresponding to population growth after agriculture is invented," Hawks said in a telephone interview.

Do you often forget appointments, have difficulty getting things in order when you need to perform a task that requires organization, or delay starting a project that you know will require a lot of thought?.

Are you ever fidgety when you must sit for long periods of time?. Do you consider yourself disorganized?. Are you easily bored?. Do you crave carbohydrates or caffeine? Have you had many different jobs, or have you experienced performance difficulties at work or disorganization at home (is your clutter out of control)? Do you frequently catch yourself finishing other people's sentences, or answering their questions before they have finished asking them?. These symptoms are frequently associated with attention deficit disorder or attention deficit hyperactivity disorder - disorders that are not just a childhood problem..

ADD/ADHD occurs in adults as well and can lead to difficulties with attention, organization, impulse control, and management of time and money.. Familial and social relationships can be affected.